The observations that benzene is metabolized to a series of phenolic compounds and causes inhibition of erythropoiesis are well documented. However, a correlation between the two events is not well established. We have observed that administration of phenol and catechol is also capable of inhibiting erythropoiesis as measured by inhibition of 59Fe incorporation into erythrocytes. We, therefore, wish to determine if other phenolic compounds, such as resorcinol, hydroquinone and quinol, resulting from benzene metabolism are also capable of suppressing erythropoiesis. In addition we propose to test the immediate precursor of catechol, benzene dihydrodiol, for bone marrow toxicity. The enzyme, benzene dihydrodiol dehydrogenase, will also be examined to determine its distribution in various tissues and whether its activity is increased by phenobarbital and 3-methylcholanthrene.